The proposed research will examine the behavioral effects of microinjections of 6-hydroxydopamine (6-OHDA), a neurotoxin capable of producing relatively specific damage to catecholaminergic pathways and terminal fields. This agent has been used previously to produce an animal analog of parkinsonism, which is thought to be a dopamine deficiency syndrome. It is proposed that this model can be made more compelling and the difference and parallels between the human and animal conditions can be made more clear through progress in behavior analysis of postural and motor aberrations. The 6-OHDA will be applied in several different doses intraventricularly or locally in the region of the ascending nigrostriatal dopaminergic systems, such that a range of severity of symptoms of catecholamine-deficiency is produced. A primary aim of the research is to test the hypothesis that subeffective brain damage in young adult rats, or effective damage from which recovery occurs, will later yield symptoms of catecholamine deficiency during old age. This effect is reminiscent of the age-dependent manifestation of symptoms in human Parkinson's Disease. The present research will lay the necessary behavioral groundwork for an understanding of this phenomenon. In addition, promising methods of control of symptoms of catecholamine deficiency will be analyzed. Particular attention will be given to the recent question of whether special feeding regimens can reduce or prevent the symptoms of catecholamine deficiency. The effects of dopamine agonists and cholinergic antagonists will be evaluated for their ability to ameliorate symptoms. The development, analysis, and control of an improved animal analog of parkinsonism (i.e., aging into symptoms that are compellingly parallel to human Parkinson's Disease) would provide an excellent preclinical means of testing the efficacy of pharmacological or other therapeutic treatment in human extrapyramidal disorders.